MiR-126/VCAM-1 regulation by naringin suppresses cell growth of human non-small cell lung cancer.

Abstract

Certain studies have indicated that naringin possesses various pharmacological activities including anti-aging, anti-oxidation, anticancer, cardiovascular and cerebrovascular disease prevention, in addition to anti-hepatic effects. The present study explores the anticancer effect of naringin on human small cell lung cancer H69AR cells. Cell growth and apoptosis rates of H69AR cells were measured by MTT or flow cytometry, which demonstrated naringin suppressed cell growth and induced apoptosis of H69AR cells. MicroRNA (miR)-126 expression and levels of phosphorylated protein kinase B (AKT), mechanistic target of rapamycin (mTOR), nuclear factor (NF)-κB and vascular cell adhesion molecule 1 (VCAM-1) proteins were detected by quantitative polymerase chain reaction and western blotting. It was identified that naringin increased miR-126 expression and suppressed the phosphorylation of AKT, mTOR, NF-κB and VCAM-1 proteins in H69AR cells. Suppression of miR-126 expression reduced the anticancer effects of naringin on H69AR cells, reversed the naringin-induced reduction of phosphoinositide 3-kinase/AKT/mTOR, and suppressed VCAM-1 protein levels. However, close of miR-126 expression did not affect the levels of NF-κB protein in H69AR cells. In summary, naringin exhibits its anti-cancer effect by suppressing cell growth of small cell lung cancer cells through miR-126/VCAM-1 signaling pathway.